INVESTIGADORES
JEREZ Susana Josefina
congresos y reuniones científicas
Título:
Platelet and fibrin network morphology alterations in a rabbit model of diet induced cardiometabolic syndrome
Autor/es:
MEDINA, MIRTA; ALARCÓN, GABRIELA; ROCO, JULIETA; MEDINA, ANALIA; ERIMBAUE, MARTA; JEREZ, SUSANA
Lugar:
Buenos Aires
Reunión:
Congreso; Reunión Conjunta de Sociedades de Biociencias; 2017
Resumen:
The cardiometabolic syndrome (CMS) is a constellation of interrelated risk factors of metabolic origins that together promote the increased risk of cardiovascular disease (CVD). Central obesity with the associated CMS components promotes proinflammatory and prothrombotic states. The aim of the present work was study whether platelet and fibrin network-morphology or coagulation profiles was altered in a rabbit model of CMS. Male rabbits were fed either a control diet (CD) or atherogenic high fat diet (18 % fat and 1 % cholesterol, HFD-HC) during 6 weeks. Methods: scanning electron microscopy was used to study platelet- and fibrin network-morphology by preparing platelet-rich plasma (PRP). Ten μl of PRP was used to study platelet morphology and 10 μl of PRP was mixed with 5 μl of bovine thrombin (2,7UI/ml) to study fibrin network morphology. Activated Partial Thromboplastin Time (APTT), thombin time and platelets count were performed. Results: Platelets of the CD appeared spherical with few pseudopodia present while the platelets of the CMS presented with numerous pseudopodia and spreading, indicating activation. The fibrin networks of the CD consist of thick and thin fibers that form an organized network of fibers. The fibrin networks of the SCM appeared less organized with less taut fibers. Fibrin fiber thickness was found to be significantly increased in the SCM group (p-value  0.05) from the CD, indicating a normal functioning coagulation cascade. Conclusion: The findings indicate that premature activation of platelets (as a result of chronic inflammation) that in turn causes altered fibrin formation but not alterations in the coagulation cascade may account for the prothrombotic status in the SCM.